R-Spondin2 CRISPR Activation Plasmid (h): sc-402648-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- R-Spondin2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- R-Spondin2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by R-Spondin2 CRISPR Activation Plasmid (h) and R-Spondin2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RSPO2 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
R-Spondin2 CRISPR Activation Plasmid (h) | sc-402648-ACT | 20 µg | $397.00 | |||
R-Spondin2 CRISPR Activation Plasmid (h2) | sc-402648-ACT-2 | 20 µg | $397.00 |
RSPO2 encodes R-Spondin2, a secreted agonist of canonical Wnt/β-catenin signaling that amplifies Wnt receptor activity through interactions with LGR4/5/6 and modulation of RNF43/ZNRF3-mediated receptor turnover. By potentiating Wnt-driven transcriptional programs, R-Spondin2 influences embryonic patterning, epithelial and mesenchymal differentiation, and tissue homeostasis, with strong relevance to processes such as morphogenesis, stem/progenitor maintenance, and barrier renewal. Dysregulated RSPO2 signaling has been associated with aberrant pathway activation in developmental defects and oncogenic contexts, making it a useful node for dissecting Wnt-dependent gene regulatory networks. Its extracellular mode of action also links RSPO2 to paracrine signaling studies in organoid, co-culture, and microenvironment-focused models.
R-Spondin2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RSPO2 expression without altering the underlying DNA sequence.
R-Spondin2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RSPO2 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the RSPO2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous R-Spondin2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RSPO2 locus and enabling the study of R-Spondin2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of R-Spondin2 pathway restoration in tumor cells with silenced or reduced RSPO2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.